Saudi Journal of Kidney Diseases and Transplantation

: 2014  |  Volume : 25  |  Issue : 4  |  Page : 900--905

Primary vesicoureteral reflux in Sudanese children

El-Tigani M. A. Ali1, Enaam M Alfaki2, Mohamed B Abdelraheem1,  
1 Department of Pediatrics and Child Health, Soba University Hospital, Faculty of Medicine, University of Khartoum, Sudan
2 Department of Paediatrics, Omdurman Teaching Hospital, Ministry of Health, Sudan

Correspondence Address:
El-Tigani M. A. Ali
Department of Pediatrics and Child Health, Soba University Hospital, Faculty of Medicine, University of Khartoum, Khartoum


Vesicoureteral reflux (VUR) is a common congenital renal tract anomaly in children. Reports from Sudan are scanty. We report the characteristics, presentation and outcome of primary VUR in a tertiary care hospital. The records of 30 patients (16 males; 53%) followed-up between January 2004 and December 2010 were reviewed. The mean age at the time of diagnosis was 4 ± 3.9 years and 47% were <2 years of age. Renal ultrasound scan (USS) failed to predict VUR in 17% of the patients. On voiding cysturethrogram (VCUG), VUR was bilateral in 57% and severe grade in 64%. Grades were not significantly associated with age, gender or site of VUR. Initial dimercaptosuccinic acid radionuclide scan showed renal damage in 61.5% of the patients. Renal damage was significantly associated with female gender and severe VUR, but not with age of onset or history of urinary tract infection (UTI). Thirteen patients (43.3%) presented with acute UTI, eight (26.6%) with non-specific urinary tract symptoms and nine (30%) with persistently elevated serum creatinine. Urine cultures were positive in 73% of patients, and E. coli was the most common pathogen. Renal impairment at presentation was significantly associated with bilateral severe VUR and history of UTI but not age or gender. After a mean follow-up period of 1.78 years (6 months to 5 years), 70% of patients remained with normal renal function and 30% progressed to chronic kidney disease; two of them died. In conclusion, our data is different from many studies. Features of primary VUR in Sudanese children are late age of onset, equal gender affection and predominance of severe grade. Presentation is associated with a high rate of UTI, renal damage and advanced renal impairment. Measures to improve early detection and treatment of VUR may reduce the risk of kidney damage.

How to cite this article:
Ali ETM, Alfaki EM, Abdelraheem MB. Primary vesicoureteral reflux in Sudanese children.Saudi J Kidney Dis Transpl 2014;25:900-905

How to cite this URL:
Ali ETM, Alfaki EM, Abdelraheem MB. Primary vesicoureteral reflux in Sudanese children. Saudi J Kidney Dis Transpl [serial online] 2014 [cited 2022 Oct 3 ];25:900-905
Available from:

Full Text


Vesicoureteral reflux (VUR) is the retrograde flow of urine from the bladder into the upper urinary tract. Primary reflux is caused by con­genital abnormality of vesicoureteral junction. It is the most common congenital urological anomaly in children, found in about 1% of newborns and as high as 30-45% of young children presenting with urinary tract infection (UTI). [1],[2],[3] Girls are more likely to have reflux than boys, [4] but in patients with prenatally de­tected hydronephrosis males were predomi­nantly affected. [5] Young infants and children <2 years of age were more likely to have VUR than older children. [6] VUR predisposes patients to acute UTI, which may lead to renal scarring. Extensive scarring may lead to further renal damage with subsequent hypertension, im­paired renal function, proteinuria and, some­times, end-stage renal failure (ESRF). [1],[7],[8] How­ever, progression to ESRF in patients with reflux has been increasingly debated. Most children with VUR present with hydroneph-rosis, often prenatally detected or with clinical UTI. Occasionally, they can present with ad­vanced reflux nephropathy (RN) manifesting as heart failure from untreated hypertension or with uremic symptoms. [9]

 Patients and Methods

We reviewed the records of all children with a diagnosis of primary VUR presenting to the Paediatric Nephrology Unit at the Soba University Hospital from January 2004 to December 2010. The diagnosis of VUR was based upon the demonstration of reflux of urine from the bladder into the upper urinary tract by contrast voiding cystourethrogram (VCUG). The grades of VUR were defined according to the International Reflux Study Group (IRSG) classification system. [10] The se­verity of VUR is classified as mild (grade I- II), moderate (III) and severe grade (IV-V). [10] UTI diagnosis was based on positive urine cul­ture with colony count of more than 100,000 colony forming units/mL of a single pathogen. Glomerular filtration rate (GFR) was estimated by the Schwartz formula and chronic kidney disease stages were defined according to the National Kidney Disease Outcome Quality Initiative guidelines. [11],[12] Chronic kidney di­sease was defined as GFR <60 mL/min/1.73 m [2] for ≥3 months with or without kidney da-mage. [13] Blood pressure values and definitions were based on the Fourth Task Force Report on the Diagnosis, Evaluation and Treatment of High Blood Pressure in Children and Ado-lescence. [14] Data collected from patients re­cords were age, gender, clinical features, labo­ratory investigations (urine cultures, serum creatinine and hemoglobin), imaging [ultra­sound scan (USS), VCUG and dimercapto-succinic acid radionuclide (DMSA) scan] and outcome measures (recovery, chronic kidney disease or death).

 Statistical Analysis

Data entry and analysis were performed using SPSS (Statistical Package for Social Sciences) version 18 was used to calculate the means and frequencies and to run the tests of significance (chi-squire tests). P-value <0.005 was consi­dered as significant.


VUR characteristics0

There were 30 children (16 male, 53.3%) with primary VUR enrolled in the study. The male to female ratio was 1.1:1, and the mean age at the time of presentation was 4 ± 3.9 years (range 4 months to 13 years). The mean age at diagnosis was younger in boys than girls (3.4 versus 4.5 years), but this was statistically insignificant, P = 0.472). Fourteen patients (47%) were below two years of age of whom nine (30%) were below one year. There was no significant gender difference between the different age groups (P = 0.68). USS showed renal tract abnormality in one or both kidneys in 25 patients (87%), i.e. USS failed to predict VUR in 17% [Table 1]. VCUG studies showed that VUR was bilateral in 17/30 patients (56.6%), giving a total of 47 refluxing ureters. Thirty of 47 (64%) refluxing ureters were severe grade (grades IV-V), four (8%) were moderate grade (grade III) and 13 (28%) were mild grade (grades I-II) [Table 2]. The asso­ciation of VUR grades were not statistically significant for age (P = 0.062), gender (P = 0.078) or site (P = 0.093). A DMSA scan was performed at the time of initial diagnosis in 13 patients (43.3%). It showed evidence of renal damage in eight of 13 patients (61.5%). Renal damage was significantly more common in females than in males (6:1, P = 0.005) and in those with severe than mild to moderate grade (7:1 versus 6:12, P = 0.0135). However, it was not significantly associated with age of onset (2.3 years versus 1.8 years, P = 0.725) or history of UTI (54% versus 46%, P = 0.416).{Table 1}{Table 2}

VUR presentation

Patterns and frequency of presentations in pa­tients with VUR are shown in [Table 3]. Thirteen patients (43.3%) presented with acute UTI, eight (26.7%) with non-specific urinary tract symptoms (bed wetting, frequency and flank pains) and nine (30%) with elevated serum creatinine. In 27 of 30 patients (90%), there was a history of recurrent UTI. Fever was reported in ten of 13 patients presenting with acute UTI. All the nine patients with high serum creatinine at presentation also had UTI. Significant growth in urine cultures was de­tected in 22 of 30 (73%) patients, and E. coli was the most common pathogen, accounting for 59% of the cultures. Other organisms were Klebsiella species in 27.5%, Pseudomonous auriginosa in 9% and Staphylococcus aureus in 4.5% of patients. Patients presenting with high serum creatinine had a mean serum crea-tinine of 3.7 mg/dL ± 2.18 (range 0.9-6.9) and a mean GFR of 18.1 ± 1.19 mL/min/1.73 m [2] (range 6.1-41). Severe anemia (Hb of 6.4 g/dL ± 3.4 SD) was diagnosed in all of the nine patients, failure to thrive in eight and hyper­tension in seven of them. Renal impairment at presentation was significantly associated with presence of bilateral VUR (P = 0.001), severe grade VUR (P = 0.003) and history of UTI (P = 0.034), but not with age or gender (P = 0.133 and P = 0.858, respectively). Characteristics of patients with normal renal function and those with impaired function at presentation are shown in [Table 4].{Table 3}{Table 4}

VUR outcome

Surgical treatment was offered to eight out of 30 patients (26.7%) of whom VUR was bila­teral in five and unilateral in three (13 refluxing ureters). In nine of 13, reflux were of severe grade (IV-V). The remaining patients were either medically treated or conservatively managed, depending on the state of their renal function. After a mean follow-up period of 1.78 ± 1.53 years (6 months to 5 years), 21 pa­tients (70%) remained with normal renal func­tion and nine (30%) progressed to chronic kidney disease (three with chronic kidney disease III-IV and six with ESRF). Two of six ESRF patients died. Ureteric reimplantation was successful in preserving normal renal function in six of eight surgically treated patients.


Primary VUR is detected in more than one third of young children presenting with UTI [1],[2],[3] and is more common in younger children, especially in infancy. [4],[15],[16] Our finding is consistent with these studies as 47% of our patients were below two years of age.

In prenatally detected VUR, males were pre­dominantly affected. [5] Conversely, in VUR de­tected by the investigation of UTI, girls were more likely to be affected. [4],[17],[18] However, other studies have shown a male predominance. [16],[19] Some other studies from a similar population of children have reported different sex ratios. [15],[20] In our series, both sexes were approximately equally affected. Therefore, this gender variation could be related to the methods of detection of VUR rather than genetic predisposition. All our patients were detected during UTI inves­tigation.

In this study, VUR was demonstrated bilate­rally in 56% of patients, which is consistent with other studies, also in Nepal (60%) and Brazil (54%). [16],[18] Many studies have shown a high incidence of lower-grade VUR, [16],[18],[21],[22] whereas other data have shown variable inci­dences of VUR grades. [15],[20] Our finding sharply contrasts with these studies as 64% of patients in this series had severe grade VUR. Many of our VUR patients were detected late with ad­vanced renal impairment and are therefore likely to have severe rather than low-grade VUR.

Although USS is used in the evaluation of pa­tients with UTI, many cases of VUR can be missed if USS is used alone for VUR screening. [15],[16],[20] In our study, USS failed to predict VUR in 17% of patients as compared with other studies from KSA and Nepal (25% and 45.8%, respectively). [15],[16] This difference could also be related to the high incidence of severe grade VUR in our series. Severe grade VUR is commonly predicted by USS than mild grade.

VUR tends to be associated with renal da­mage at diagnosis in about 30-60% of cases in some studies. [16],[21],[23],[24] In this series, the DMSA scan detected renal damage in 61% of patients at initial diagnosis. Males, especially with pre-natally detected VUR, [3],[5] and those with severe grade VUR had a higher risk of developing renal damage. [18],[21] In our study, renal damage was significantly more common in females and in those with severe grade VUR (P = 0.02 and 0.013, respectively). This finding is expected as no patient in our series was detected pre-natally. We could not find a significant asso­ciation between the incidence of renal damage and age of onset as in other studies. [17],[21],[25]

Many children with VUR present either with hydronephrosis, often prenatally detected, or with clinical UTI, which often presents with non-specific signs and symptoms. They can also present with manifestations of advanced RN or may be asymptomatic. [9] Most of our patients presented with evidence of UTI, with E. coli being the most common pathogen, which is consistent with the reports from other studies. [15],[18],[21] Thirty percent of our patients presented with advanced RN associated with severe anemia, failure to thrive and hyperten­sion. This finding contrasts sharply with other studies showing either no or a lower incidence of advanced RN at diagnosis. [15],[18],[21] However, one study from India has demonstrated ad­vanced RN in more than 75% of their young adults with VUR. [26] In our series, advanced RN was significantly associated with bilateral se­vere grade VUR and UTI but not with age or gender. Bilateral severe grade VUR in the presence of recurrent UTI is likely to lead to RN if remained undetected.

Follow-up VCUG was not performed for most of our patients, as many parents did not agree for a repeat procedure. The follow-up period was relatively short. However, surgery was successful in preserving normal renal function in six of eight patients having bila­teral severe grade VUR. Despite prophylaxis and surgery, about 30% of our patients progressed to chronic kidney disease, mostly ESRF. It is likely that such high incidence of CKD is due to failure of early detection of VUR in the presence of recurrent UTI.

Our study was not without limitations. This study was a retrospective study in which some data may not be accurately collected. The rela­tively small number of patients in a hospital-based study may not precisely reflect the whole spectrum of VUR features. However, the study provides information about this important health problem.

In conclusion, our data are different from that in western and some developing countries ha­ving better facilities. Characteristics of primary VUR in Sudanese children were late age of onset, equal gender affection and predomi­nance of severe grades. Presentation is asso­ciated with a high incidence of UTI, renal da­mage and advanced renal impairment. Despite surgery, about one-third of patients remained with chronic kidney disease or died. Efforts directed toward improving early detection and treatment of this disorder may reduce the risk of renal damage. Training of doctors on UTI management guidelines and introduction of protocols for prenatal detection of VUR may help in the early detection and management of such patients.


This work is a part of a Thesis submitted for partial fulfillment of Clinical MD in Pediatrics, University of Khartoum, 2010. The authors thank all the staff in the Medical Records Departments in the Soba University Hospital for helping with data collection. Their thanks are extended to the Health Statistic Depart­ment, University of Khartoum, for help with data analysis.


1Dillon MJ, Goonasekera CD. Refax nephropathy. J Am Soc Nephrol 1998;9:2377-33.
2Shan KJ, Robins DG, White RH. Renal scarring and vesicoureteric reflux. Arch Dis Child 1978; 53:210-7.
3Smellie JM, Normand IC, Katz G. Children with urinary infection: A comparison of those with and those without vesicoureteric reflux. Kidney Int 1981; 20:717-22.
4Weiss R, Tamminen-Mobius T, Koskimies O, et al. Characteristics at entry of children with severe primary vesicoureteral reflux recruited for a multicenter, international therapeutic trial com-paring medical and surgical management. The International Reflux Study in Children. J Urol 1992;148:1644-9.
5Yeung CK, Godley ML, Dhillon HK, Gordon I, Duffy PG, Ransley PG. The characteristics of vesicoureteric refax in male and female infants with prenatal hydronephrosis. Br J Urol 1997;80: 319-27.
6Skoog SJ, Peters CA, Arant BS Jr, et al. Pediatric Vesicoureteral Reflux Guidelines Panel Summary Report: Clinical Practice Guidelines for Screening Sibling of children with Vesicoureteral Reflux and Neonates/Infants with Prenatal Hydronephrosis. J Urol 2010;184:1145-51.
7Elder JS, Peters`CA, Arant BS Jr, et al. Pediatric Vesicoureteral Reflux Guidelines Panel summary report on the management of primary vesico-ureteral reflux in children. J Urol 1997;157:1846-51.
8Willi U, Treves S. Radionuclide voiding cysto-graphy. Urol Radiol 1983;5:161-73, 75.
9Available from: http://emedicine:medscape.Com/article/101439- clinical [Last accessed on 2/2/2012].
10Medical versus surgical treatment of primary vesicoureteral reflux: Report of the International Reflux Study Committee. Pediatrics 1981;67: 392-400.
11Schwartz GJ, Brion LP, Spitzer A. The use plasma creatinine concentration for estimating glomerular filtration rate in infants, children and adolescents. Pediatr Clin North Am 1987;34:571-90.
12Belman AB. Vesicoureteric reflux. Pediatr Clin North AM 1997;44:1171-90.
13Hogg KJ, Furth S, Lemely KV, et al. National Kidney Foundation′s Kidney Disease Quality Initiative clinical practice guidelines for chronic kidney disease in children and adolescence: evaluation, classification, and stratification. Pediatrics 2003;111:1416-21.
14The Fourth Report on the Diagnosis, Evaluation, and Treatment of High Blood Pressure in Children and Adolescents. NIH Publication No. 05-5267. Originally printed September 1996 (96-3790) Revised May 2005.
15AL Mohrj OA, AL Zaben AA, AL Rasheed S. Vesicoureteral reflux in children. Experience in Riyadh, Saudi Arabia. Saudi J Kidney Dis Transpl 1996;7:301-4.
16Shrestha S, Basukala S, Pokhrel N. Primary vesicoureteric reflux in Nepalese children. Kathmandu Univ Med J (KUMJ) 2008;6:75-8.
17Skoog SJ, Belman AB, Majid M. A nonsurgical approach to the management of primary vesicoureteral reflux. J Urol 1987;138:941-6.
18Silva JM, Diniz JS, Oliveira EA, et al. Features of primary vesicoureteral reflux and renal damage in children at a single institution in Brazil from 1969 to 1999. Int Urol Nephrol 2003;35:161-8.
19Wang Z, Xu H, Liu HM, Rao J, Shen Q, Cao Q. Clinical analysis of 139 cases of primary vesicoureteric reflux in children. Zhonghura er ke za zhi. Chin J Pediatr 2008;46:518-21.
20Al-Ibrahim AA, Girdharilal RD, Jalal MA, Alghamdy AH, Ghazal YK. Urinary tract infec-tion and vesicoureteral reflux in Saudi children. Saudi J Kidney Dis Transpl 2002;13:24-8.
21Shabaf FG, Fallahzadeh MH, Modarresi AR, Esmaeilli M. Primary vesicoureteral reflux in Iranian children. Indian Pediatr 2007;44:128-30.
22Vachvanichsanog P, Dissaneewate P, Lim A. Characteristics of primary vesico-ureteral reflux in Thai children. Pediatr Int 2008;50:363-6.
23Smellie JM, Normand IC. Bacteruria, reflux, and renal scarring. Arch Dis Child 1975;50:581-5.
24Shaikh N, Ewing AL, Bhatnagar S, Hoberman A. Risk of renal scarring in children with first urinary tract infection: A systemic review. Pediatrics 2010;126:1084-91.
25Caione P, Ciofetta G, Collura G, Morano S, Capozza N. Renal damage in vesico-ureteric reflux. BJU Int 2004;93:591-5.
26Sakhuja V, Muthukumar T, Sud K, et al. Vesicoureteric reflux and reflux nephropathy as seen at a tertiary care adult nephrology service in India - an analysis of 86 patients. Ren Fail 2003;25:173-81.